Now onto enhancing CJC-1295 to blow it into the next universe of effects.

CJC-1295 is the perfect foundation for doing this. Because it lasts 24 hours a day for 8-10 days straight. Whereas GHRH, which does the same signalling of the GHSR, only lasts 7 minutes.

First its important to understand how GH surges work. Pay especial attention to Somatostatin.

When a secretagogue of GH, such as GHRH, Ghrelin, Hexarelin, or CJC-1295, signals the GHSR it causes the pituitary to release HGH, IF, Somatostatin levels are low enough to allow it. Once a surge of GH is released, Somatostatin levels will rise up again, thus even if something is binding to the GHSR, it CANNOT signal the release of GH because Somatostatin levels are too high.

Somatostatin is what controls the negative feedback mechanisms of GH release in the pituitary. After a surge of GH is released from a secretagogue wether natural or man-made, Somatostatin levels will rise, preventing further GH release until the GH levels decrease, at which point the ultra-short feedback mechanisms of the hypothalamus-pituitary-axis (HPA) kick in and cause Somatostatin levels to decrease.

The moment somatostatin levels decrease sufficiently, more GH can be released. However under natural conditions, there wont be sufficient GHRH remaining at the GHSR to cause more GH release once Somatostatin levels decrease. Because GHRH is also released in surges, and only lasts 7 minutes upon its circulating release.

However because CJC-1295 lasts 24 hours a day for 8-10 days, its ALWAYS at the GHSR, so the moment somatostatin levels decrease enough, another surge of GH will happen because CJC-1295 is there binding to the GHSR's. Therefore under naturakl endocrine system, you'd get lets say 5 surges of GH a day. Whereas with CJC-1295, youd get lets say 15 surges of GH a day.

So whats the obvious limiters of GH release?? Well first, is the duration of GHRH or whatever GHS is signaling the release. This has been overcome with CJC-1295.

Whats the second limiter? Somatostatin. Somatostatin is an inhibitor of GH release. Not so easy to fix??? WRONG! This is where I come in.

Amazingly, no one that ive seen has realized this. That is, if you could inhibit Somatostatin levels while using CJC-1295, you would allow the CJC-1295 to signal an ENDLESS surge of GH (so long as the body was producing sufficient peptide, which means you need a high protein diet since peptides are made from amino acids in protein). Yes, thats not a typo, an ENDLESS surge of GH. The equivalent of strapping an IV bag of HGH to your back and walking around all-day with a drip of GH into you. The difference between the "surge" system and that would be night and day. Im not saying its the healthiest or safest thing to do, but it is so far beyond the natural endocrine function it will lead to results never before experienced or even imagined with HGH of any kind or any way previously available. I can vouch for this as ive been experimenting with this recently.

There is a class of compounds called Acetylcholineesterase inhibitors, that inihibit acetylcholineesterase, which is responsible for deactivating acetylcholine in the brain. Guess what? Acetylcholine is a very effective inhibitor of Somatostatin. Therefore Acetylcholineesterase inhibitors are indirect somatostatin inihibitors, working by increasing acetylcholine levels which then inhibit somatostatin levels.

Does this really work? YES, its been clinically proven in numerous studies with stunning results. In the studies they used GHRH + Acetylcholineesterase inhibitor Pyrostigmine at a dosage of 120mg. Remember GHRH only lasts 7 minutes, so they only get a single surge of GH from using it. What the study found is that orally administering Pyrostigmine, an acetylcholineesterase inhibitor, and then injecting GHRH vs. the placebo/control group resulted in a dramatically larger amount of GH released in response to the same dosage of GHRH. This is because somatostatin levels were dramatically lowered, and allowed an even larger amount of GH to be released in response to GHRH.

Had the study used CJC-1295 they wouldve had a far greater result. Not only would more GH be released per surge, but they wouldve had an endless or damn near endless surge of GH release, rather than the normal "Pulsatile" release system which is controlled by:

A) The short duration of GHRH and other endogenous secretagogues (overcome with CJC-1295)

B) The GH-inhibitory action of Somatostatin (overcome with acetylcholineesterase inhibitors)

Acetylcholineesterase inhibitors are taken orally, they are legal and readily available for purchase as they are extracted from natural plant sources. They are CHEAP, costing just a dollar or less per day to use in conjunction with CJC-1295. By taking them you can use a lower CJC-1295 dosage and still get much greater results. It totally changes the pituitary system into what I must call the uber-pituitary.

Normally the pituitary functions like this;
1) Endogenous GH secretagogue such as GHRH or Ghrelin, signals pituitary to release HGH, the amount of GH released is controlled by somatostatin and GHRH quantity.
2) Pituitary releases HGH creating a 'surge', immediately after, somatostatin levels rise thus making the pituitary unresponsive to GHRH or other secretagogues, GHRH remaining becomes deactivated due to proteocyltic cleavage.
3) After the HGH released has become deacticated by the body, Somatostatin levels begin to decrease again, and once more endogenous secretagogues arrive, another surge will occur and repeat process.

The pituitary function using CJC-1295 + a somatostatin inhibitor (in this case acetylcholineesterase inhibitors), functions like this:
1) Exogenously supplied GH secretagogue CJC-1295 signals pituitary to release HGH, the amount of GH released is GREATER than without acetylcholineesterase inhibitor due to suppression of somatostatin.
2) Pituitary releases HGH creating a surge, however, somatostatin levels fail to rise after the release, therefore the pituitary remains responsive to secretagogues to signal more release of HGH, and the CJC-1295 fails to degrade due to its design thus lasting 24 hours a day for 8-10 days from an injection.
3) After the HGH is released, ANOTHER surge is immediatley signalled by the still active CJC-1295, and then another surge, and another, and another, and another, and another, and in the time span that 1 natural surge wouldve happened and another would be ready to go, probably 20x as many surges have already occured.

So for just 50 extra cents a day and the consumption of an oral pill of a legal, readily available compound, you can ABSURDLY modify the pituitary response to CJC-1295 by suppressing Somatostatin. YOUVE BEEN WARNED, this is INSANELY potent, beyond the design of humanity. BE CAREFUL!

NOTICE, Huperzine A dosage is in the MICROgrams NOT MILLIgrams. If you took 50mg of Huperzine A you would DIE. I use Huperzine A myself for this. But you can use any of the above, perhaps pyrostigmines better because thats what was proven effective in the clinical studies at that specific dosage. But all three of the above are acetylcholineesterase inhibiors and will thuis have the same inhibitory impact on somatostatin.

This is how, for just an extra 50 cents to a dollar a day, you can turn CJC-1295 into the physiological equivalent of strapping an IV bag of HGH to your back and having a 24 hour drip. As you can imagine this is ABSURDLY POWERFUL and needs great respect and caution when you first begin experimenting. Start with a low CJC-1295 dosage and a low acetylcholineesterase inhibitor dosage, and work from there based on your experiences.

EVERYONE should do this. It gives you FAAAAAAAAAAR more bang for your buck from the CJC-1295, and costs just cents per day to do ontop of CJC-1295 use. Its supported fully by clinical studies, just search for the pyrostigmine/GHRH study.

Ageforce rep, Lets patch up those mistakes and stop going oral.
Knowledge is power- The power to do your part and make a difference.

So Do I use bsw or aa? I was thinking pinning once a week for 4 pins a month.

you dont use use cjc 1295 DAC alone. You still have to use a GHRP. ipam, GHRP2 whatever....you still need one to get the pulse. The DAC is not as bad as it is made out to be. Yes it does cause GH Bleed, but you only use it for 8,10 or 12wks you will return to normal shortly after.

You just dont want to stay on it for 6-8 months at a time. Using DAC for 8wks, than non DAC or mod GRF or cjc 1293 for 8wks, than go back to DAC.

Lots of peptide info you will find online is older, when they first hit the scene everyone was talking about them. Fast forward to today and you have a lot of conflicting information out there. It was not until recently (6months - 1 yr back) did we learn the the GH bleed is caused by the DAC (Drug affinty complex) and this is not ideal since is the same as a womens GH output.

So for a long time, yrs even, everyone talked up cjc 1295 DAC....now we find out different.

Huperzine = less Somatostatin...I realize this is now an old article but i would love to hear about results anyone has had using DAC and Huperzine to draw down Somatostatin?regaurdless of dac or no dac wouldn't Huperzine be valuable to both peps?

well have been dosing 100mcg with ipam cjc. Nothing to report as of yet, at least no "wow hot damm this is the golden ticket" but realizing peps are a long term go i was not expecting much right away. All i have to go on is the recommendation from others.